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Two TAL effectors of Xanthomonas citri pv. malvacearum target GhSWEET15 as the susceptibility genes for bacterial blight of cotton
by
Huang, Kunxuan
, Ali Shah, Syed Mashab
, Xu, Xiameng
, Haq, Fazal
, Wang, Yong
, Khojasteh, Moein
, Xu, Zhengyin
, Li, Ying
, Chen, Gongyou
, Wang, Qi
, Liu, Linlin
, Khan, Asaf
, Yang, Ruihuan
in
Pathology
2024
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Two TAL effectors of Xanthomonas citri pv. malvacearum target GhSWEET15 as the susceptibility genes for bacterial blight of cotton
by
Huang, Kunxuan
, Ali Shah, Syed Mashab
, Xu, Xiameng
, Haq, Fazal
, Wang, Yong
, Khojasteh, Moein
, Xu, Zhengyin
, Li, Ying
, Chen, Gongyou
, Wang, Qi
, Liu, Linlin
, Khan, Asaf
, Yang, Ruihuan
in
Pathology
2024
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Two TAL effectors of Xanthomonas citri pv. malvacearum target GhSWEET15 as the susceptibility genes for bacterial blight of cotton
by
Huang, Kunxuan
, Ali Shah, Syed Mashab
, Xu, Xiameng
, Haq, Fazal
, Wang, Yong
, Khojasteh, Moein
, Xu, Zhengyin
, Li, Ying
, Chen, Gongyou
, Wang, Qi
, Liu, Linlin
, Khan, Asaf
, Yang, Ruihuan
in
Pathology
2024
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Two TAL effectors of Xanthomonas citri pv. malvacearum target GhSWEET15 as the susceptibility genes for bacterial blight of cotton
Paper
Two TAL effectors of Xanthomonas citri pv. malvacearum target GhSWEET15 as the susceptibility genes for bacterial blight of cotton
2024
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Overview
Bacterial Blight of Cotton (BBC) caused by Xanthomonas citri pv. malvacearum (Xcm) is an important and destructive disease affecting cotton plants. Transcription activator-like effectors (TALEs) released by the pathogen regulate cotton resistance to the susceptibility. In this study, we sequenced the whole genome of Xcm Xss-V2-18 and identified eight tal genes; seven on the plasmids and one on the chromosome. Deletion and complementation experiments of Xss-V2-18 tal genes demonstrated that Tal1b is required for full virulence on cotton. Transcriptome profiling coupled with TALE-binding element prediction revealed that Tal1b targets GhSWEET15A04/D04 and GhSWEET15D02 simultaneously. Expression analysis confirmed the independent inducibility of GhSWEET15A04/D04 and GhSWEET15D02 by Tal1b, whereas GhSWEET15A04/D04 is additionally targeted by Tal1. Moreover, GUS (β-glucuronidase) and Xa10-mediated HR (hypersensitive response) assays indicated that the EBEs are required for the direct and specific activation of the candidate targets by Tal1 and Ta1b. These findings may advance our understanding of the dynamics between TALEs and EBEs, and decipher a simple and effective DNA-binding mechanism that could lead to the development of more efficient methods for gene editing and transgenic research.
Publisher
Cold Spring Harbor Laboratory
Subject
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